Preussmann R
Zentralbl Bakteriol Orig B. 1978 Mar;166(2-3):144-58.
New aspects on the mechanism of action of known environmental carcinogens are described. These compounds are not active as such, but are bioactivated in the mammalian metabolism via chemically reactive intermediates to electrophilic reactants, forming with information-bearing biopolymeres covalent bonds. This change in the genetic code is in agreement with the mutation hypothesis of carcinogenesis. Aflatoxin B1, N-nitroso compounds and benzo(a)pyrene are taken as examples. "Threshold levels", e.g. no-effect-levels derived from animal experiments with all their inherent limitations, are compared with data from human exposure to benzo(a)pyren, aflatoxine, N-nitroso compounds and vinyl chloride. The difficulties of such risk evaluations are discussed.
文中描述了已知环境致癌物作用机制的新观点。这些化合物本身并不具有活性，而是在哺乳动物代谢过程中通过化学反应性中间体生物活化成为亲电反应物，与携带信息的生物聚合物形成共价键。这种遗传密码的改变与致癌作用的突变假说相符。以黄曲霉毒素B1、N-亚硝基化合物和苯并(a)芘为例。将“阈值水平”，如源自动物实验的无效应水平及其所有固有局限性，与人类接触苯并(a)芘、黄曲霉毒素、N-亚硝基化合物和氯乙烯的数据进行了比较。讨论了此类风险评估的困难。
